Bacterial lipopolysaccharide induces mRNA expression of an IκB MAIL through toll-like receptor 4
Bacterial lipopolysaccharide induces mRNA expression of an IκB MAIL through toll-like receptor 4
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DOI：
10.1292/jvms.64.419
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发表时间：
2002-05-01
影响因子：
1.2
通讯作者：
Saito, M
中科院分区：
文献类型：
--
作者：
Kitamura, H;Kanehira, K;Saito, M
具有脂多糖诱导的锚定重复序列的分子（MAIL）是最近被鉴定为在给予细菌脂多糖（LPS）后出现在免疫活性器官中的分子的核IkappaB蛋白。研究了LPS受体的主要形式Toll样受体（TLR）4在LPS诱导的MAIL表达中的参与。当人骨髓单核细胞系U937用佛波醇12-肉豆蔻酸酯13-乙酸酯处理3天时，LPS诱导的MAIL表达与TLR 4表达的增加平行地增强。当用抗TLR 4的中和抗体处理细胞时，MAIL诱导作用减弱。在脾脏中的MAIL的体内诱导在具有错义突变的Tlr 4基因的小鼠中比在正常对照小鼠中小。这些结果共同表明，TLR 4至少部分有助于LPS刺激后的MAIL诱导。
Molecule possessing ankyrin-repeats induced by lipopolysaccharide (MAIL) is a nuclear IkappaB protein recently identified as a molecule appearing in immunocompetent organs after administration of bacterial lipopolysaccharide (LPS). Participation of Toll-like receptor (TLR) 4, which is a major form of LPS receptors, in the LPS-induced MAIL expression was investigated. When a human myelomonocytic cell line U937 was treated with phorbol 12-myristate 13-acetate for 3 days, the LPS-induced MAIL expression was much potentiated in parallel with an increase in TLR4 expression. The MAIL induction was attenuated when the cells were treated with a neutralizing antibody against TLR4. The in vivo induction of MAIL in the spleen was smaller in mice having a missense mutation of the Tlr4 gene than in normal control mice. These results collectively indicate that TLR4 contributes, at least in part, MAIL induction after LPS stimulation.